Mānuka oil is an essential oil derived from Leptospermum scoparium, a plant that has been used by the indigenous populations of New Zealand and Australia for centuries. Both the extracted oil and its individual components have been associated with various medicinal properties. Given the rise in resistance to conventional antibiotics, natural products have been targeted for the development of antimicrobials with novel mechanism of action. This review aimed to collate available evidence on the antimicrobial, anti-parasitic and anti-inflammatory activities of mānuka oil and its components. A comprehensive literature search of was conducted using PubMed and Embase (via Scopus) targeting articles from database inception until June 2020. Chemical structures and IUPAC names were sourced from PubChem. Unpublished information from grey literature databases, Google search, targeted websites and Google Patents were also included. The present review found extensive in vitro data supporting the antimicrobial effects of mānuka oil warrants further clinical studies to establish its therapeutic potential. Clinical evidence on its efficacy, safety and dosing guidelines are necessary for its implementation for medical purposes. Further work on regulation, standardization and characterization of the medicinal properties of mānuka oil is required for establishing consistent efficacy of the product.

Rhinoviruses (RVs) are the etiological agents of upper respiratory tract infections, particularly the common cold. Infections in the lower respiratory tract is shown to cause severe disease and exacerbations in asthma and COPD patients. Viruses being obligate parasites, hijack host cell pathways such as programmed cell death to suppress host antiviral responses and prolong viral replication and propagation. RVs are non-enveloped positive sense RNA viruses with a lifecycle fully contained within the cytoplasm. Despite decades of study, the details of how RVs exit the infected cell are still unclear. There are some diverse studies that suggest a possible role for programmed cell death. In this review, we aimed to consolidate current literature on the impact of RVs on cell death to inform future research on the topic. We searched peer reviewed English language literature in the past 21 years for studies on the interaction with and modulation of cell death pathways by RVs, placing it in the context of the broader knowledge of these interconnected pathways from other systems. Our review strongly suggests a role for necroptosis and/or autophagy in RV release, with the caveat that all the literature is based on RV-A and RV-B strains, with no studies to date examining the interaction of RV-C strains with cell death pathways.

Parkinson’s disease (PD) is an irreversible neurodegenerative disorder clinically manifesting in uncontrolled motor symptoms. There are two primary hallmark features of Parkinson’s disease—an irreversible loss of dopaminergic neurons of the substantia nigra pars compacta and formation of intracellular insoluble aggregates called Lewy bodies mostly composed of alpha-synuclein. Using a clinical improvements-first approach, we identified several clinical trials involving consumption of a specific diet or nutritional supplementation that improved motor and nonmotor functions. Here, we aimed to investigate if and how pyrroloquinoline quinone (PQQ) compound disrupts preformed alpha-synuclein deposits using SH-SY5Y cells, widely used Parkinson’s disease cellular model. SH-SY5Y neuroblastoma cells, incubated in presence of potassium chloride (KCl) to induce alpha-synuclein protein aggregation, were treated with PQQ for up to 48 hr. Resulting aggregates were examined and quantified using confocal microscopy. Overall, nutritional compound PQQ reduced the average number and overall size of intracellular cytoplasmic alpha-synuclein aggregates in a PD cellular model.